Renal Vascular Resistance and Aortic Pressure as Determinants of Sodium Reabsorption

During induced renal vasodilatation, angiotensin and norepinephrine result in an increased excretion of sodium (UNaV), which has been attributed to transmission of elevated aortic pressure (PA) to peritubular capillaries and not to direct effects of the drugs on sodium reabsorption. The importance of PA, intrarenal hemodynamics, and other possible effects of angiotensin and norepinephrine was examined in anesthetized dogs in which one kidney was vasodilated by denervation or acetylcholine, and the opposite kidney served as control. During elevation of aortic pressure, following bilateral carotid occlusion and vagotomy (B.C.O. and V), infusion of angiotensin and norepinephrine, increased UNaV occurred on only the vasodilated side. Changes in UNaV on both sides are related inversely to renal vascular resistance (R.V.R.) before elevation PA, but not to changes in R.V.R., glomerular filtration rate (G.F.R.), or filtration fraction following elevation of PA. When renal perfusion pressure was controlled during ...